Feeding behavior provides the metabolic fuels essential for life. Disturbances of its regulation can have severe consequences for the individual. Insufficient feeding can jeopardize reproduction and survival. On the other hand, excessive feeding can increase the probability of diabetes, hypertension, and heart disease. Therefore, understanding the role of the nervous system in the regulation of feeding is an important goal for basic science. We believe, as did Sherrington, that the most fruitful approach to analyzing the system as a whole begins at the anatomical level(s) of the relevant sensory inputs and motor outputs. For the feeding system, many of the relevant sensory inputs taste, trigeminal, visceral) enter, and all of the consummatory motor outputs (somatic and autonomic) emerge, at the level of the caudal brainstem (CBS). We developed a chronic decerebrate rat model to test whether these CBS circuits, in neural isolation from the forebrain, can perform a range of ingestive control functions seen in the intact rat. The experiments in the present proposal continue to investigate the ingestive behavior of the chronic decerebrate rat. The proposed experiments will: (1) Investigate the linkage between sensory (taste and postingestive) stimuli and oral motor output that may provide the substrate for the regulation of individual meals. (2) Distinguish between the contribution of gastric and postgastric signals to satiation and the control of meal size. Gastric emptying and the gastric and postgastric distributions of ingested glucose will be measured at the end of intraoral meals. (3) Determine the necessity of the forebrain for long-term caloric homeostasis by examining whether the decerebrate rat adjusts the size of individual meals in response to regulatory challenges such as alterations in meal frequency and caloric density. Whether or not decerebrate and intact rats differ, the results obtained will help delineate the anatomical boundaries of the feeding control circuitry. Experiments that reveal a disruption of ingestion control in the chronic decerebrate will highlight the interaction between forebrain and CBS mechanisms of ingestion control. Failures to uncover differences between decerebrate and intact rats will be dramatic and, as in the past, will stimulate investigations of the location, connectivity and physiology of the relevant CBS integrative circuits.